Our research program is concerned with developing and testing models of how cognitive processes are mediated in the human brain. This is accomplished via studies of patients with brain injury and disease, and via studies of normal individuals using functional brain imaging modalities. Our previous studies of semantic memory in patients with Alzheimer's disease (AD) suggest that posterior cortical pathology results in a degradation of previously acquired knowledge. These degraded knowledge representations are, in turn, proposed to be responsible for word-finding problems, and to substantially contribute to poor memory in patients with AD. Studies completed this past year revealed that these patients have a specific difficulty processing motion verbs. This finding suggested a relative specific deficit in the automatic activation of stored information about concepts defined by single features (e.g., motion) relative to concepts defined by multiple features (e.g., concrete objects). In contrast, automatic activation of more global information (e.g., how frequently events occur in the environment) was found to be intact, even though AD patients were unable to explicitly retrieve this information from memory. Using magnetic resonance imaging, we have obtained evidence that priming, a form of implicit learning that is preserved in patients with amnesia and in patients with AD, is mediated by decreased neural activity in specific brain regions, whereas explicit memory is mediate by increased activity throughout the same brain network. In addition, using positron emission tomography we demonstrated that the medial region of the temporal lobe, an area known to play a critical role in establishing new memories, is automatically engaged whenever an event is experienced. Moreover, the side and amount of activity in this region is modulated by stimulus characteristics (form, meaning) and task experience.